ASF1B enhances migration and invasion of lung cancers cell via regulating the P53-mediated epithelial-mesenchymal transformation (EMT) signaling pathway

Wang, Wei; Xiao, Li‐Na; Pan, Deng; Hu, Lingzhi

doi:10.4149/neo_2021_210818n1181

Cited by 12 publications

(8 citation statements)

References 19 publications

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“…Another co-expressed gene, NUSAP1 , is also recognized as an independent risk factor for HCC patient outcome, and regulates the expression of CDK4, CDK6, and cyclinD1, which participate in cell cycle progression [ 29 ]. Similar results have shown that ASF1B promotes aggressive features of invasion and metastasis in lung cancer cells via the p53 signaling pathway [ 30 ]. In addition, studies have confirmed that the positively correlated co-expression genes NUSAP1 , ASF1B , TPX2 , and SKA1 are invariably involved in immune cell infiltration in numerous cancers, and thus contribute to the regulation of the tumor immune microenvironment [ 29 , 31 – 33 ].…”

Section: Discussionsupporting

confidence: 78%

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

Cheng,

Liu,

Chang

et al. 2024

Eur J Med Res

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Background The WD40 repeat (WDR) domain provides scaffolds for numerous protein–protein interactions in multiple biological processes. WDR domain 76 (WDR76) has complex functionality owing to its diversified interactions; however, its mechanism in LGG has not yet been reported. Methods Transcriptomic data from public databases were multifariously analyzed to explore the role of WDR76 in LGG pathology and tumor immunity. Laboratory experiments were conducted to confirm these results. Results The results first confirmed that high expression of WDR76 in LGG was not only positively associated with clinical and molecular features of malignant LGG, but also served as an independent prognostic factor that predicted shorter survival in patients with LGG. Furthermore, high expression of WDR76 resulted in the upregulation of oncogenes, such as PRC1 and NUSAP1, and the activation of oncogenic mechanisms, such as the cell cycle and Notch signaling pathway. Finally, WDR76 was shown to be involved in LGG tumor immunity by promoting the infiltration of immune cells, such as M2 macrophages, and the expression of immune checkpoints, such as PDCD1 (encoding PD-1). Conclusions This study shows for the first time the diagnostic and prognostic value of WDR76 in LGG and provides a novel personalized biomarker for future targeted therapy and immunotherapy. Thus, WDR76 may significantly improve the prognosis of patients with LGG.

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Section: Discussionsupporting

confidence: 78%

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

Cheng,

Liu,

Chang

et al. 2024

Eur J Med Res

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“…Next, it was found that interference with ASF1B in Res186 cells could remarkably halt cell proliferation, metastasis and stimulate cell cycle arrest and apoptosis in LGG in our study. ASF1B could enhance the migratory as well as invasive capabilities of lung cancer cells via the modulation of p53-mediated epithelial-mesenchymal transformation signalling pathway [ 27 ]. MiR-214 inhibited the proliferative ability and promoted the apoptotic rate of myeloma cells by down-regulating ASF1B [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

The interaction between ASF1B and TLK1 promotes the malignant progression of low-grade glioma

Zhang

Liu

2023

Annals of Medicine

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Aim Low-grade glioma (LGG), which is the second most frequent adult brain malignancy, severely threatens patients’ health and has a high recurrence rate. Histone H3/H4 chaperone anti-silencing function 1 B ( ASF1B ) has a tight association with the initiation and development of tumours. The expression and regulation mechanism of ASF1B in LGG were discussed. Methods ASF1B expression in LGG patients as well as the association of ASF1B with overall survival and disease-free survival of LGG patients were predicted by GEPIA database. The independent prognostic value of ASF1B in LGG patients was investigated by TCGA database. RT-qPCR, together with western blot was applied for the assessment of ASF1B in LGG cell lines. After ASF1B expression was inhibited, CCK8 and colony formation assays judged cell proliferation. Flow cytometry analysis and TUNEL assay appraised cell cycle as well as apoptosis. Cell migratory and invasive capacities were measured by wound healing as well as Transwell assays. Western blot tested the expression of proliferation-, cycle-, apoptosis-, and metastasis-associated proteins. STRING and GeneMANIA database predicted the relationship between ASF1B and tousled-like kinase 1 ( TLK1) . ChIP assay testified the affinity of ASF1B with TLK1. Subsequently, TLK1 was overexpressed and ASF1B expression interfered, and the functional assays were executed. Results ASF1B was discovered to be increased in LGG tissues and cells and indicates an unfavourable prognosis for LGG patients. ASF1B was not an independent prognostic factor for LGG. ASF1B deficiency obstructed the proliferation, cell cycle as well as metastasis of LGG cells, and induced cell death, which might be realized through the interaction with TLK1 . Conclusion The interaction between ASF1B and TLK1 promoted the malignant progression of LGG. Key messages TLK1 interacts with ASF1B. Interference with ASF1B inhibits the proliferative, invasive and migratory capabilities and induces the cycle arrest, along with the apoptosis of LGG cells. The interaction between ASF1B and TLK1 promotes the malignant progression of LGG.

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“…Finally, one last additional pathway of interest is represented by p53, through its links with various drivers of EMT discussed in other chapters of this review. A first report described the importance of a chaperone protein of histone H3-H4, the anti-silencing function 1 (ASF1B), which promotes cell proliferation, migration, and invasion through the modulation of the p53mediated EMT signaling pathway (Wang et al, 2022). Secondly, Pustovalova et al shed light on the crosstalk between autophagy and this pathway (Pustovalova et al, 2021).…”

Section: Major Findings Relevant To Other Signaling Pathwaysmentioning

confidence: 99%

Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies

et al. 2022

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Curcuminoids, which include natural acyclic diarylheptanoids and the synthetic analogs of curcumin, have considerable potential for fighting against all the characteristics of invasive cancers. The epithelial-to-mesenchymal transition (EMT) is a fundamental process for embryonic morphogenesis, however, the last decade has confirmed it orchestrates many features of cancer invasiveness, such as tumor cell stemness, metabolic rewiring, and drug resistance. A wealth of studies has revealed EMT in cancer is in fact driven by an increasing number of parameters, and thus understanding its complexity has now become a cornerstone for defining future therapeutic strategies dealing with cancer progression and metastasis. A specificity of curcuminoids is their ability to target multiple molecular targets, modulate several signaling pathways, modify tumor microenvironments and enhance the host’s immune response. Although the effects of curcumin on these various parameters have been the subject of many reviews, the role of curcuminoids against EMT in the context of cancer have never been reviewed so far. This review first provides an updated overview of all EMT drivers, including signaling pathways, transcription factors, non-coding RNAs (ncRNAs) and tumor microenvironment components, with a special focus on the most recent findings. Secondly, for each of these drivers the effects of curcumin/curcuminoids on specific molecular targets are analyzed. Finally, we address some common findings observed between data reported in the literature and the results of investigations we conducted on experimental malignant mesothelioma, a model of invasive cancer representing a useful tool for studies on EMT and cancer.

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ASF1B enhances migration and invasion of lung cancers cell via regulating the P53-mediated epithelial-mesenchymal transformation (EMT) signaling pathway

Cited by 12 publications

References 19 publications

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

WD repeat domain 76 predicts poor prognosis in lower grade glioma and provides an original target for immunotherapy

The interaction between ASF1B and TLK1 promotes the malignant progression of low-grade glioma

Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies

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